cns general reactions to injury - university … • robbins basic pathology. kumar et al....
TRANSCRIPT
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CNS GENERAL REACTIONS TOINJURY
Reid Hefner, M.D.Department of Pathology and Anatomical
SciencesTuesday, November 7, 2017
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LEARNING OBJECTIVES
• Review normal gross CNS anatomy• Be familiar with normal cells in CNS• Know special stains used in neuropathology• Understand basic CNS reactons to injury• Know in what conditons a reacton occurs • Know defnitons discussed in lecture
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REFERENCES
• Robbins Basic Pathology. Kumar et al.Pathologic Basis of Disease. 9th Editon.Saunders, Philadelphia, 2015. Chapter 28.
• Robbins 9th editon, 2013, Chapter 22• Or Robbins 10th editon, 2017, Chapter 23
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MACROSCOPIC EXAM
• The enlarged brain– Difuse=edema– Hydrocephalus-early*– Mass lesion(s)– May create increased intracranial pressure
• The small brain– Atrophic processes
• Hydrocephalus-late*– Destructve processes
• The focal lesion– Infarcts
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BRAIN EDEMA
normal
edema
Compare the ventricles for sizeCompare the sulci for width
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Brain edema-CT scan
Ventricles are slit-like
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BRAIN EDEMA
Widened gyri
Narrow sulci
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BRAIN EDEMA-CAUSES
• Trauma• Tumor• Stroke• Metabolic• Infecton
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BRAIN EDEMA-MECHANISMS
• Cytotoxic-intracellular– Membrane permeability is increased
• Vasogenic-extracellular– Leaky hose=↑ vascular permeability
• Transependymal-extracellular– Increased ventricular pressure
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CYTOTOXIC EDEMA
Cells appear vacuolated
Intracellular fluid
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VASOGENIC EDEMA
The leaky pipe principle
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VASOGENIC EDEMA
• Most common type• Located mainly in white
mater– Cytotoxic in gray mater
• Causes– Tumor– Stroke– Abscess– Trauma
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What is wrong?
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HYDROCEPHALUS
• Acute or chronic• High pressure
– Block in ventricular fow– Block in meningeal circulaton– Block in reabsorpton
• Normal pressure– Hydrocephalus Ex vacuo
About 500 ml CSFproduced each day
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Ventral brain
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Brain-lateral view
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CSF drainage system
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HYDROCEPHALUS
CLINICAL PROBLEM OFDILATED VENTRICLES
Hydrocephalus vs atrophy
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TRANSEPENDYMAL EDEMA
• Rapid elevaton ofventricular pressure
• Fluid crosses ependymalbarrier
• Concentrated aroundventricles
• Brain is large
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MASS LESIONSThe brain is enlarged
Cerebral Hemorrhage
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BRAIN EDEMA/HYDROCEPHALUS/MASS LESION-CONSEQUENCES
• Raised intracranial pressure (RIP)– Diminished cerebral blood fow→ ischemia
• Herniatons– Shifs within the cranial cavity
• Compression of third nerve and cerebellar tonsils• Blood vessel damage in pons
• Pressure rises exponentally once all theextra-axial spaces are flled
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HERNIATIONSComplicatons of edema and/or mass
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Uncal herniaton
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Increased intracranial pressure
Fixed dilated pupilParasympathetic fibers compromised
Pressure on third cranial nerve
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What’s happening here?
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IIP-DURET HEMORRHAGES
• Downward movement ofpons
• Stretching of the pontnevessels
• Secondary brainstemhemorrhages result
• Coma, death ensue
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RAISED IP-TONSILLAR HERNATION
Herniation throughforamen magnum
Compression ofmedulla
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RAISED IP-TONSILLAR HERNATION
Herniation intoforamen magnum
Compression ofmedulla
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RIP and EDEMA-TREATMENT
• Shuntng of CSF from ventricles• Acetazolamide
– Reduce CSF producton (temporary)• Mannitol
– Osmotcally remove fuid from brain• Cortcosteroids
– Works in vasogenic edema– Reduces synthesis of prostaglandins– Seems to reduce vascular dilaton and permeability
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ATROPHIC BRAINAlzheimer’s Disease
Widened sulci
Normal sulci
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ATROPHIC BRAIN Alzheimer’s Disease
Hydrocephalus ex vacuo
Normal ventricles
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DESTRUCTIVE LESIONSOld Infarct
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FOCAL LESIONSLacunar Infarcts
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MICROSCOPIC EXAM
• Neurons• Axons • Neuropil and myelin• Glia• Ependyma • Meninges
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CELLULAR REACTIONS
• Injury or death• Regeneraton • Proliferaton or hyperplasia• Atrophy or cell loss• Inclusions• Storage• Neoplasia
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SPECIAL STAINS INNEUROPATHOLOGY
• Nissl (cresyl violet)– Ribosomes in neurons
• Luxol fast blue (LFB)– Myelin stains blue
• PTAH-not used anymore– Astrocytc processes stained with metallic tungstc acid
• Cajal (Nobel Prize)-not used diagnostcally– Gold impregnaton for astrocytes
• Silver stains (e.g. Bodian)– Nerve processes– Several types of inclusions, senile plaques
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Cast of characters
• Nero the neuron• Astrocyte• Oligodendroglia• Microglia• Pac(man) the macrophage• Expendable the ependymal
cell
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Cells of the brain
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Nero the neuron
I’m pretty special because I’m like an emperor
All cells pay homage to me-astrocytes dote on me
Pear-shaped histologically
Too lazy to have offspring-no regeneration
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Olive the oligodrocyte
Loves myelinMakes and maintains
Myelin
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Aster the astrocyte
Dotes on Nero
Provides support to Nero
Has offspring=proliferation during injury
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Mike the microglia
Fights his way between theendothelial cells and the glial cells
Battles disease and the Democrats
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Cast of characters
Pac(man) the macrophage
Pretty feisty
Eats everything in sight
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Expendable the ependymal cell
This boring cell doesn’t react much
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NEURONS
• Cells do not regenerate or proliferate– But axon may regenerate or sprout
• Necrosis• Apoptosis• Atrophy• Chromatolysis• Inclusions• Storage
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NORMAL NEURON
Vesicular nucleusProminent nucleolusAbundant ribosomesAxonMicrofilaments/tubulesSynapses
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NORMAL NEURON
Pear-shaped
Nissl substance
Nucleolus
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Not all neurons are created equal
Internal granular layer
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NISSL SUBSTANCE
Rough ER
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NORMAL NEURON
Silver stain (Bodian) shows Neuroflaments and neurotubules neuronal processes
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ACUTE NEURONAL INJURY
apoptosis
necrosis
normal
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Mechanisms of Cell DeathFrequently inter-related
• Reduced energy– ↓ ATP, glucose, oxygen
• Mitochondrial damage– May lead to apoptosis
• Membrane damage– ↑ permeability
• Free radicals
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INCLUSIONS
• Accumulatons of virus or proteins• Causes
– Misfolding of normal protein– Accumulaton of abnormal protein– Autophagic actvity
• Ofen seen as hyaline or flamentous material withincell– Usually eosinophilic in H&E stains– Glassy and homogeneous
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NEURONAL ATROPHY
Atrophy in aging
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INCLUSIONS
viral
tangle
Neurofibrillary tangle
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AUTOPHAGIC VACUOLES
Granulovacuolar change in hippocampus in aging
Also seen are neurofibrillary tangle and neuritic plaque
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Granulovacuolar change
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AUTOPHAGYGranulovacuolar change
• Debris in cell• Then surrounded
by membrane• Fuses with
lysosome to formautophagic vacuole
• Debris may bedegraded/removed
• Can trigger celldeath by complex& somewhatunknownmechanism
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NEURONAL STORAGE-LIPID
Tay-Sachs disease
Ganglioside storage due to hexosaminidase Adeficiency
Membranous cytoplasmic bodies
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NEURONAL LOSS
Normal cerebellum
Loss of granular layer cells andPurkinje cells
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AXONS AND DENDRITES
• Wallerian degeneraton• Spheroids (swollen axons)• Segmental demyelinaton• Axonal sproutng
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NEURON AND PROCESSES
• Disease targets– Neuron
• Wallerian-afer neuron dies• Spheroid
– Axon• Wallerian-afer axon is cut• Spheroid
– Myelin• Demyelinaton
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WALLERIAN DEGENERATION
• Severe axonal injuryor afer neuron dies
• Changes occur distalto injury
• Axonal atrophy &break-up of myelin
Myelin stain
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WALLERIAN DEGENERATION
• Axon shrinks (blackarrow)
• Myelin debris withphagocytosis
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ALS-Tract degeneraton
Rob. Fig. 28-39
LFB stain
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AXONAL SPHEROIDS
• Axon swollen• Causes-sublethal injury
– Trauma– Aging– Near an infarct– Toxins
• Vincristne
Bodian silver stain
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AXONAL SPHEROIDS
• Axonal transport slows/stops• Distended axon• Myelin may be intact, at least
early• Axons contain
– ↑ Filaments– Other organelles accumulate– Debris collects
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Peripheral Nerve Injury
• Segmental demyelinaton=primary myelin disease– Remyelinaton with onion bulbs
• Axonal injury– May be secondary to myelin loss– May be Wallerian with axonal atrophy
• Myelin ovoids– May produce spheroids– Ofen induces axonal sproutng
• This probably also occurs in CNS too
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Teased nerve fbers
Axons stained withosmium
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PERIPHERAL NERVE-TEASED FIBERS
Myelin stained with osmium tetroxide (black)
Normal (1), demyelinated (2) and remyelinated axons (3)
1
2
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Segmental Demyelinaton
• Segments of myelin lost– Between internodes
typically• Causes
– Guillain-Barré syndrome– Diabetes
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REMYELINATION
NORMAL NERVE
ONION BULBS
Schwann cells proliferateEncircle demyelinated axon
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Onion bulb
Rob. Fig. 27-5
Spiraling Schwann cells
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AXONAL INJURY WITH MYELINOVOIDS
Myelin breaks down (ovoids) after axonal injury
More diffuse, not segmental
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Axonal sproutng
Axon injury
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NEUROPIL AND MYELIN
• Neuropil is the background in the grey mater– Neuritc plaques– Spongiform change
• Myelin is abundant in the white mater– Primary demyelinaton-multple sclerosis– Secondary demyelinaton-infarcton
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NEUROPIL
Senile (neuritc) plaque (Bodian) CJ Disease (spongiform)
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MYELIN
MS plaque
NORMAL LFB STAIN
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ASTROCYTES
• Proliferate to form a glial scar– Increased cellularity (see only nuclei)
• Cytoplasmic swelling (gemistocytes)• Elaboraton of processes• Inclusions
– Rosenthal fbers, Alzheimer II cells • Neoplasia
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NORMAL ASTROCYTE
CAJAL GOLD STAIN
STARS IN SKY
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NORMAL GLIA
Oligos look likelymphocytes
Astrocytes havelarger, vesicular(open) nuclei
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ASTROCYTES
Glial fbrillaryAcidic protein (GFAP)
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GLIOSISCNS’s answer to fbrosis
Increased astrocytes seen as increased numbers of nuclei
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GLIOSIS
Gemistocytes ([Gr] gemistos)Astrocyte cytoplasm is “swollen or hypertrophic”
Seen in early gliosis but can remain for months
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Gemeste or Greek stuffed pepper
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FIBRILLARY GLIOSIS
Glial processes form a scar (PTAH)
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ASTROCYTE INCLUSIONS
Rosenthal fbersSeen in long term gliosis, especially inbenign childhood astrocytomas
Masses of intermediate filaments
Contain αβ-crystalline and ubiquitin
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Alzheimer type II astrocytes
Nothing to do with Alzheimer’s diseaseType of reactive astrocyte seen in hepatic diseaseNucleus enlarged and clear
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ASTROCYTE type II INCLUSIONS
Alz II cell
Seen in liver diseasewith ↑ serum NH3
Nucleus enlarged, clear,contains glycogen
Alzheimer I cell larger,multiple nuclei, visiblecytoplasm
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OLIGODENDROGLIA
• Make and maintain myelin• Limited regeneraton/Limited remyelinaton• Vacuolizaton• Inclusions• Damage and loss→demyelination
– Ischemia, MS, PML• Neoplasia
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OLIGODENDROCYTES
Major dense line (dark)=inner membrane
Intraperiod line=extracellular space
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OLIGODENDROCYTES
LFB stain showing myelinated areas
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OLIGODENDROCYTES
Satellite oligos
Near neurons
Rows of oligos in white matter
NORMAL BRAIN
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OLIGODENDROCYTES
Cytoplasmic vacuoles in (cytotoxic) edema
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OLIGODENDROCYTES
Intranuclear viral inclusions in PML
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OLIGODENDROCYTENecrosis
Eosinophilic cytoplasm with fuzzy nucleus
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MICROGLIA
• Derived mainly from monocytes inblood
• Begin as rod cells→ giter cells• Proliferate at site of injury• Difuse in large lesions• Focal lesions
– Neuronophagia– Glial nodules
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MICROGLIAThe “Unglia”-Not really glia
Monocytes enter brain from blood
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MICROGLIA
Rod cells frstFlaten out to travelbetween axons andother cell processes
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Pacman the macrophage
Pac Man eats everything in sight
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PHAGOCYTIC MICROGLIA
Gitter cells (macrophages)
Cytoplasm resembles a lattice
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MICROGLIA
Neuronophagia Glial nodulesPhagocytotosis of neurons in apoptosis Focal clusters of microglia et al
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EPENDYMAL CELLSThe pathologically boring cell that doesn’t react much
• Ependyma keeps CSF within ventricles• Limited regeneratve or reactve potental• Cell loss
– Hydrocephalus, infecton– Ependymits granularis (actually astrocytc gliosis)
• Infecton/infammaton– From meningits– CMV infecton
• Neoplasia
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NORMAL EPENDYMA
Ciliatedepithelium
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EPENDYMAL CELLS
Ependymits granularis Proliferaton of subependymal astrocytesSeen afer hydrocephalus or infammaton of the ventricles
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CMV infecton of ependyma
CMV loves ependyma
Intranuclear andcytoplasmic inclusions
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MENINGES: DURA AND PIA-ARACHNOID
• Blood or infammatory cells may beseen in these spaces
• Fibrosis of the leptomeninges• Tumors
– Meningiomas
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MENINGES
Pia-arachnoid (leptomeninges)
Focal hyperplasia ofarachnoid
Derived from neuralcrest
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MENINGEAL FIBROSIS
• Causes– Aging– Meningits– Bleeding
• Consequences– Slows CSF circulaton or
reabsorpton– May result in
hydrocephalus
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MENINGESMeningioma
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THE END
Raymond Cajal
Franz Nissl
Augustus Waller
del Rio Hortega